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Acute Coronary Syndrome
Dr. Nathan Muluberhan (MD+ , Assi. professor of EMCC, HrU School of
Medicine Dean & CPD Director of BHE)
Objectives
• To know and describe different types of ACS
• To know risk factors, sign and symptoms of patients with ACS
• To know the ECG manifestation of ACS
• To the initial stabilization and management of patients with ACS
Acute Coronary Syndrome
• Acute coronary syndrome (ACS) refers to the constellation of
clinical diseases occurring as a result of acute myocardial ischemia.
• ACS includes a spectrum of clinical presentations ranging from
unstable angina (UA) to acute myocardial infarction (AMI).
• Sudden cardiac death (SCD) is the most extreme form of ACS.
• Unstable angina: considered to be an ACS in which there is
myocardial ischemia without detectable myocardial necrosis.
Characterized by- symptom occurring at rest/with minimal exertion, lasting>10
min; severe & of a new onset; crescendo pattern (i.e. more severe, prolonged, or
frequent than previously).
Acute Coronary Syndrome
Acute myocardial infarction (AMI): defined by myocardial necrosis
with elevation of cardiac biomarkers and is classified by ECG findings
as:
1. ST-segment elevation myocardial infarction(STEMI): Chest pain >20 to
30 min occurring at rest (not relieved by nitroglycerin), serologic evidence
of myonecrosis, and persistent ST-segment elevation.
2. Non-ST-segment elevation myocardial infarction (NSTEMI): UA with
evidence of myocardial necrosis (elevated cardiac biomarkers)
Acute Coronary Syndrome
Risk Factors
Modifiable Non-Modifiable
• Increasing age
• Gender (male)
• Ethnicity
• Family History
• ?Diabetes
• Smoking
• Obesity
• Diet
• Lack of exercise
• High serum cholesterol
• Hypertension
HISTORYAND ASSOCIATED SYMPTOMS
Chest discomfort or pain
• Substernal or in the left chest, with radiation to the arm (either), neck, or jaw.
• Chest pressure, heaviness, tightness, fullness, or squeezing.
• Less commonly, patients describe their symptoms as knife-like, sharp, or
stabbing
• Associated symptoms such as nausea, vomiting, diaphoresis, dyspnea,
lightheadedness, syncope, and palpitations.
PHYSICAL EXAMINATION
• The pulse rate may be normal or fast, slow or irregular.
• Bradycardic (poor prognostic sign) rhythms are more common with
inferior wall myocardial ischemia
• An S3 is present in 15% to 20% of patients with AMI.
• The presence of a new systolic murmur is an ominous sign because
it may signify papillary muscle dysfunction.
DIAGNOSIS
• The diagnosis of STEMI depends on the ECG in the setting of
symptoms suggestive of MI.
• The diagnosis NSTEMI depends on abnormal elevation of cardiac
biomarkers but may include ECG changes not meeting criteria for
STEMI.
• The diagnosis of unstable angina is based on history because the
ECG and cardiac injury biomarkers are nondiagnostic.
• Early risk assessment for the likelihood of myocardial infarction uses
all of these data to aid decision making.
• Exercise, stress, and a cold environment classically precipitate angina.
• Angina typically has a duration of symptoms of <10 minutes,
• occasionally lasting up to 10 to 20 minutes, and usually improves within 2 to 5
minutes after rest or nitroglycerin.
• In contrast, AMI is usually accompanied by more prolonged and
severe chest discomfort, more prominent associated symptoms.
• Easy fatigability may be a prominent symptom of ACS, especially in
women.
HISTORYAND ASSOCIATED SYMPTOMS
Diagnosis
• The diagnosis of ST-segment elevation myocardial infarction
(STEMI) depends on the ECG in the setting of symptoms suggestive
of myocardial infarction.
• The diagnosis of non-ST-segment elevation myocardial infarction
(NSTEMI) depends on an abnormal elevation of cardiac biomarkers
but may include ECG changes not meeting the criteria for STEMI.
• The diagnosis of unstable angina is based on history: Angina pain
with at least 1 of 3 features: Occurs at rest/with minimal exertion or
lasting>10 min, Severe & of a new onset or crescendo pattern (i.e.
more severe, prolonged, or frequent than previously).
ECG
ECG: done at presentation; repeat at 6–12 h& with any change in
symptoms
• UA/NSTEMI= ST depression/transient elevation or deep T inversion
(>=0.3mV)
• STEMI=New ST elevation in 2 contiguous leads >= 0.2 mV in men or
0.15 mV in women in leads V2-3 and/or 0.1mV in other leads OR new
LBBB
• N.B the ECG must also be analyzed for rate, rhythm,etc (look for
arrhythmias)
Cardiac Biomarkers
• Serial testing at presentation & 6–12 h after symptom onset.
• Cardiac troponins ( T&I) rise 20 -50 Xs Upper normal limit/UNL/ in
acute MI; rise 4-8 hr after injury; may remain elevated for 7-10 days;
more Specific & Sensitive than CK-MB
• Creatine kinase (CK )-rises in 4–8 hr; normalize by 48–72 h; lacks
specificity
Other investigation
• Echocardiography: may show new wall motion abnormality
• RBS, electrolytes, OFTs, lipid profiles
• CXR: to look for pulmonary edema; R/o other DDx (PTE, pneumonia,
Pneumothorax...)
• Coronary angiography if indicated
Management
• Should focus on stabilizing the patient's condition,
• relieving ischemic pain, and
• providing antithrombotic therapy to reduce myocardial damage and
prevent further ischemia.
• The goal is early revascularization.
1) General measures: Continuous ECG monitoring for arrhythmia & ST
changes
• V/S: Q 2 hr until stable, then Q 4hr & as needed
• O2 (2-4 lit/min) if SaO2<90%
• Bed rest, Sedation, VTE(venous thrombo-embolism) prophylaxis
• NPO except for sips of water until stable; IV fluid – e.g. For inferior MI
• Glycemic control-goal is RBS of 140-180mg/dl(if > 180mg/dl,give regular
• Insulin-1-2IU for each 50mg/dl increase above 180mg/dl, by measuring
RBS Q 6hrs)
• Treat comorbidities like DM (for both types-standing doses of lente /NPH
2) Medications:
• Aspirin(ASA): loading:162–325 mg chewed, then 75–162 mg/d plus
• Clopidogrel: loading: 300mg Po, then 75 mg/d for at least 1 yr (but
ASA lifelong)
• Nitroglycerin (NTG): sublingual 0.4 mg Q 5 min as needed or
persistent chest pain *IV NTG for persistent ischemia .C/I= low BP,
sildenafil use
• Morphine sulphate sulfate: 2–5 mg IV, may be repeated Q 5–30 min
as needed to relieve Symptoms (can also use morphine syrup,
pethidine or tramadol)
• Metoprolol: 25–50 mg PO q 6 h* (If HTN, ongoing pain, tachycardia: give
IV over 1–2 min by 5mgincrements. If not available- use atenolol,
propranolol/carvedilol. C/I- CHF, bradycardia.
• UFH: Bolus 60–70 U/kg (max. 50000 IU) IV then infusion of 12–15 U/kg/
h (initial Maximum 1000 U/h) titrated to aPTT 50–70 s * If no per fuser,
12,500U SC BID is possible; OR LMWH (Enoxaparin):1 mg/kg SC Q 12
h(if GFR< 30,1mg/kg once daily)
• Statins: atorvastatin 80mg PO/d is preferred. Others options are pravastatin/
Simvastatin/ lovastatin 40mg Po/day
• ACEIs: start low dose eg. Enalapril /lisinopril 2.5 to 5mg po/d OR captopril
6.25-12.5mg TID; then escalate gradually to clinically effective dose.
• Invasive therapy in ACS: for a high risk patients who present early,
referral to a better set up is recommended (If the patient can afford)
• Time since onset of symptoms- 90 min for PCI / 12 hours for fibrinolysis
• Determine if fibrinolysis candidate- Meets criteria with no contraindications
• Determine if PCI candidate- Based on availability and time to balloon
treatment
• STEMI: Fibrinolysis Vs PCI/CABG
• Unstable angina/NSTEMI: PCI/ CABG; but fibrinolysis is not indicated.

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Acute Coronary Syndrome presentation and management.pptx

  • 1. Acute Coronary Syndrome Dr. Nathan Muluberhan (MD+ , Assi. professor of EMCC, HrU School of Medicine Dean & CPD Director of BHE)
  • 2. Objectives • To know and describe different types of ACS • To know risk factors, sign and symptoms of patients with ACS • To know the ECG manifestation of ACS • To the initial stabilization and management of patients with ACS
  • 3. Acute Coronary Syndrome • Acute coronary syndrome (ACS) refers to the constellation of clinical diseases occurring as a result of acute myocardial ischemia. • ACS includes a spectrum of clinical presentations ranging from unstable angina (UA) to acute myocardial infarction (AMI). • Sudden cardiac death (SCD) is the most extreme form of ACS.
  • 4. • Unstable angina: considered to be an ACS in which there is myocardial ischemia without detectable myocardial necrosis. Characterized by- symptom occurring at rest/with minimal exertion, lasting>10 min; severe & of a new onset; crescendo pattern (i.e. more severe, prolonged, or frequent than previously). Acute Coronary Syndrome
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  • 6. Acute myocardial infarction (AMI): defined by myocardial necrosis with elevation of cardiac biomarkers and is classified by ECG findings as: 1. ST-segment elevation myocardial infarction(STEMI): Chest pain >20 to 30 min occurring at rest (not relieved by nitroglycerin), serologic evidence of myonecrosis, and persistent ST-segment elevation. 2. Non-ST-segment elevation myocardial infarction (NSTEMI): UA with evidence of myocardial necrosis (elevated cardiac biomarkers) Acute Coronary Syndrome
  • 7. Risk Factors Modifiable Non-Modifiable • Increasing age • Gender (male) • Ethnicity • Family History • ?Diabetes • Smoking • Obesity • Diet • Lack of exercise • High serum cholesterol • Hypertension
  • 8. HISTORYAND ASSOCIATED SYMPTOMS Chest discomfort or pain • Substernal or in the left chest, with radiation to the arm (either), neck, or jaw. • Chest pressure, heaviness, tightness, fullness, or squeezing. • Less commonly, patients describe their symptoms as knife-like, sharp, or stabbing • Associated symptoms such as nausea, vomiting, diaphoresis, dyspnea, lightheadedness, syncope, and palpitations.
  • 9. PHYSICAL EXAMINATION • The pulse rate may be normal or fast, slow or irregular. • Bradycardic (poor prognostic sign) rhythms are more common with inferior wall myocardial ischemia • An S3 is present in 15% to 20% of patients with AMI. • The presence of a new systolic murmur is an ominous sign because it may signify papillary muscle dysfunction.
  • 10. DIAGNOSIS • The diagnosis of STEMI depends on the ECG in the setting of symptoms suggestive of MI. • The diagnosis NSTEMI depends on abnormal elevation of cardiac biomarkers but may include ECG changes not meeting criteria for STEMI. • The diagnosis of unstable angina is based on history because the ECG and cardiac injury biomarkers are nondiagnostic. • Early risk assessment for the likelihood of myocardial infarction uses all of these data to aid decision making.
  • 11. • Exercise, stress, and a cold environment classically precipitate angina. • Angina typically has a duration of symptoms of <10 minutes, • occasionally lasting up to 10 to 20 minutes, and usually improves within 2 to 5 minutes after rest or nitroglycerin. • In contrast, AMI is usually accompanied by more prolonged and severe chest discomfort, more prominent associated symptoms. • Easy fatigability may be a prominent symptom of ACS, especially in women. HISTORYAND ASSOCIATED SYMPTOMS
  • 12. Diagnosis • The diagnosis of ST-segment elevation myocardial infarction (STEMI) depends on the ECG in the setting of symptoms suggestive of myocardial infarction. • The diagnosis of non-ST-segment elevation myocardial infarction (NSTEMI) depends on an abnormal elevation of cardiac biomarkers but may include ECG changes not meeting the criteria for STEMI. • The diagnosis of unstable angina is based on history: Angina pain with at least 1 of 3 features: Occurs at rest/with minimal exertion or lasting>10 min, Severe & of a new onset or crescendo pattern (i.e. more severe, prolonged, or frequent than previously).
  • 13. ECG ECG: done at presentation; repeat at 6–12 h& with any change in symptoms • UA/NSTEMI= ST depression/transient elevation or deep T inversion (>=0.3mV) • STEMI=New ST elevation in 2 contiguous leads >= 0.2 mV in men or 0.15 mV in women in leads V2-3 and/or 0.1mV in other leads OR new LBBB • N.B the ECG must also be analyzed for rate, rhythm,etc (look for arrhythmias)
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  • 19. Cardiac Biomarkers • Serial testing at presentation & 6–12 h after symptom onset. • Cardiac troponins ( T&I) rise 20 -50 Xs Upper normal limit/UNL/ in acute MI; rise 4-8 hr after injury; may remain elevated for 7-10 days; more Specific & Sensitive than CK-MB • Creatine kinase (CK )-rises in 4–8 hr; normalize by 48–72 h; lacks specificity
  • 20. Other investigation • Echocardiography: may show new wall motion abnormality • RBS, electrolytes, OFTs, lipid profiles • CXR: to look for pulmonary edema; R/o other DDx (PTE, pneumonia, Pneumothorax...) • Coronary angiography if indicated
  • 21. Management • Should focus on stabilizing the patient's condition, • relieving ischemic pain, and • providing antithrombotic therapy to reduce myocardial damage and prevent further ischemia. • The goal is early revascularization.
  • 22. 1) General measures: Continuous ECG monitoring for arrhythmia & ST changes • V/S: Q 2 hr until stable, then Q 4hr & as needed • O2 (2-4 lit/min) if SaO2<90% • Bed rest, Sedation, VTE(venous thrombo-embolism) prophylaxis • NPO except for sips of water until stable; IV fluid – e.g. For inferior MI • Glycemic control-goal is RBS of 140-180mg/dl(if > 180mg/dl,give regular • Insulin-1-2IU for each 50mg/dl increase above 180mg/dl, by measuring RBS Q 6hrs) • Treat comorbidities like DM (for both types-standing doses of lente /NPH
  • 23. 2) Medications: • Aspirin(ASA): loading:162–325 mg chewed, then 75–162 mg/d plus • Clopidogrel: loading: 300mg Po, then 75 mg/d for at least 1 yr (but ASA lifelong) • Nitroglycerin (NTG): sublingual 0.4 mg Q 5 min as needed or persistent chest pain *IV NTG for persistent ischemia .C/I= low BP, sildenafil use • Morphine sulphate sulfate: 2–5 mg IV, may be repeated Q 5–30 min as needed to relieve Symptoms (can also use morphine syrup, pethidine or tramadol)
  • 24. • Metoprolol: 25–50 mg PO q 6 h* (If HTN, ongoing pain, tachycardia: give IV over 1–2 min by 5mgincrements. If not available- use atenolol, propranolol/carvedilol. C/I- CHF, bradycardia. • UFH: Bolus 60–70 U/kg (max. 50000 IU) IV then infusion of 12–15 U/kg/ h (initial Maximum 1000 U/h) titrated to aPTT 50–70 s * If no per fuser, 12,500U SC BID is possible; OR LMWH (Enoxaparin):1 mg/kg SC Q 12 h(if GFR< 30,1mg/kg once daily) • Statins: atorvastatin 80mg PO/d is preferred. Others options are pravastatin/ Simvastatin/ lovastatin 40mg Po/day • ACEIs: start low dose eg. Enalapril /lisinopril 2.5 to 5mg po/d OR captopril 6.25-12.5mg TID; then escalate gradually to clinically effective dose.
  • 25. • Invasive therapy in ACS: for a high risk patients who present early, referral to a better set up is recommended (If the patient can afford) • Time since onset of symptoms- 90 min for PCI / 12 hours for fibrinolysis • Determine if fibrinolysis candidate- Meets criteria with no contraindications • Determine if PCI candidate- Based on availability and time to balloon treatment • STEMI: Fibrinolysis Vs PCI/CABG • Unstable angina/NSTEMI: PCI/ CABG; but fibrinolysis is not indicated.

Editor's Notes

  1. ; if detected, an S3 may indicate a failing myocardium.